Method and system for terminating an atrial arrhythmia
Abstract
A method and system is provided for responding, from internally within a patient, to an atrial arrhythmia in a heart including measuring from within the patient at least one electrocardiogram characteristic indicative of the atrial arrhythmia, and controlling from within the patient drug therapy delivery to the patient responsive to measuring the at least one electrocardiogram characteristic. Drug therapy is initiated to the patient responsive to measuring the at least one electrocardiogram characteristic. According to one aspect of the present invention, the drug therapy is staged within the patient prior to measuring the at least one electrocardiogram characteristic. According to another example embodiment, the heart is paced from within the patient at a predefined rate responsive to measuring the at least one electrocardiogram characteristic, pacing occurring alone, or in combination with drug therapy.
Claims
exact text as granted — not AI-modified1. A method of responding, from internally within a patient, to an atrial arrhythmia in a heart, the method comprising:
monitoring electrocardiograms indicative of cardiac activity within the heart;
measuring from within the patient at least one electrocardiogram characteristic indicative of the atrial arrhythmia;
initiating a drug delivery therapy responsive to the indicated atrial arrhythmia; and
controlling from within the patient the drug therapy delivery to the patient responsive to indications of ventricular proarrhythmia from the monitored electrocardiogram.
2. The method of claim 1 , further comprising:
pacing the heart from within the patient at a predefined rate responsive to measuring at least one electrocardiogram characteristic after initiating drug therapy delivery.
3. The method of claim 1 , further comprising initiating drug therapy delivery to the patient responsive to measuring the at least one electrocardiogram characteristic, the drug therapy being staged within the patient prior to measuring the at least one electrocardiogram characteristic.
4. The method of claim 3 , wherein controlling the drug delivery therapy further comprises preventing the initiation of the drug therapy delivery to the patient that was responsive to measuring the at least one electrocardiogram characteristic, the drug therapy being staged internal to the patient prior to measuring the at least one electrocardiogram characteristic.
5. The method of claim 4 , wherein drug therapy includes an anti-arrhythmic drug.
6. The method of claim 5 , wherein the anti-arrhythmic drug includes Ibutilide.
7. The method of claim 4 , wherein the at indication of ventricular proarrhythmia includes a Q–T interval.
8. The method of claim 7 , wherein the indication of ventricular proarrhythmia is that the Q–T interval is greater than 480 mS.
9. The method of claim 1 , further comprising:
pacing the heart from within the patient at a predefined rate responsive to measuring the at least one electrocardiogram characteristic and prior to initiating the drug delivery therapy.
10. The method of claim 9 , wherein controlling includes signaling the patient to initiate drug therapy delivery responsive to measuring the at least one electrocardiogram characteristic.
11. The method of claim 10 , wherein the at least one electrocardiogram characteristic includes a time duration difference between a monitored Q–T interval and a selected Q–T interval duration range.
12. The method of claim 9 , further comprising initiating drug therapy delivery to the patient responsive to the at least one electrocardiogram characteristic, the drug therapy being staged internal to the patient prior to the atrial arrhythmia.
13. The method of claim 12 , wherein drug therapy delivery includes delivering an anti-arrhythmic drug.
14. The method of claim 13 , wherein the anti-arrhythmic drug includes Ibutilide.
15. The method of claim 12 , wherein the at least one electrocardiogram characteristic includes a time duration difference between a monitored Q–T interval and a selected Q–T interval duration range.
16. The method of claim 15 , wherein initiating drug therapy delivery to the patient is responsive to the time duration difference being within the selected duration range.
17. The method of claim 9 , further comprising signaling the patient to terminate drug therapy delivery responsive to the indication of ventricular proarrhythmia.
18. The method of claim 17 , wherein the indication of ventricular proarrhythmia includes a time duration difference between a monitored Q–T interval and a selected Q–T interval duration range.
19. The method of claim 18 , wherein signaling the patient to terminate drug therapy delivery is responsive to the time duration difference being outside the selected duration range.
20. The method of claim 17 , wherein the indication of ventricular proarrhythmia includes a time duration difference between a Q–T interval monitored after initiating drug therapy delivery and a Q–T interval monitored prior to initiating drug therapy delivery.
21. The method of claim 20 , further comprising signaling the patient to terminate drug therapy delivery is responsive to the time duration difference being greater Than 500 mS, the Q–T interval monitored after initiating drug therapy delivery being of greater duration than the Q–T interval monitored prior to initiating drug therapy delivery.
22. The method of claim 17 , wherein the indication of ventricular proarrhythmia includes Q–T interval variability.
23. The method of claim 22 , further comprising signaling the patient to terminate drug therapy delivery responsive to Q–T interval variability exceeding a selected threshold Q–T interval variability after initiating drug therapy delivery.
24. The method of claim 22 , further comprising signaling the patient to terminate drug therapy delivery responsive to Q–T interval variability measured after initiating drug therapy delivery exceeds Q–T interval variability measured prior to initiating drug therapy delivery by at least 50%.
25. The method of claim 17 , wherein the indication of ventricular proarrhythmia includes frequency of ventricular ectopy.
26. The method of claim 25 , further comprising signaling the patient to terminate drug therapy delivery responsive to a frequency of ventricular ectopy exceeding a selected threshold frequency of ventricular ectopy after initiating drug therapy delivery.
27. The method of claim 25 , further comprising signaling the patient to terminate drug therapy delivery responsive to a frequency of ventricular ectopy measured after initiating drug therapy delivery exceeds a frequency of ventricular ectopy measured prior to initiating drug therapy by at least 50%.
28. The method of claim 9 , wherein pacing the heart includes pacing a ventricle at a rate that exceeds a spontaneous ventricular rate.
29. The method of claim 9 , further comprising alerting the patient that at least one ventricle is in arrhythmia after terminating the drug therapy delivery.
30. The method of claim 29 , where controlling the drug delivery therapy further comprises internally terminating the drug therapy delivery responsive to the indication of ventricular proarrhythmia.
31. The method of claim 30 , wherein the indication of ventricular proarrhythmia includes a time duration difference between a monitored Q–T interval and a selected Q–T interval duration range.
32. The method of claim 31 , wherein internally terminating drug therapy delivery is responsive to the time duration difference being outside the selected duration range.
33. The method of claim 30 , wherein the indication of ventricular proarrhythmia includes a time duration difference between a Q–T interval monitored after initiating drug therapy delivery and a Q–T interval monitored prior to initiating drug therapy delivery.
34. The method of claim 33 , further comprising internally terminating drug therapy delivery to the patient responsive to the time duration difference being greater than 480 mS, the Q–T interval monitored after initiating drug therapy delivery being of greater duration than the Q–T interval monitored prior to initiating drug therapy delivery.
35. The method of claim 30 , wherein the indication of ventricular proarrhythmia includes Q–T interval variability.
36. The method of claim 35 , further comprising internally terminating drug therapy delivery to the patient responsive to Q–T interval variability exceeding a selected threshold Q–T interval variability after initiating drug therapy delivery.
37. The method of claim 35 , further comprising internally terminating drug therapy delivery to the patient responsive to Q–T interval variability measured after initiating drug therapy delivery exceeds Q–T interval variability measured prior to initiating drug therapy delivery by at least 50%.
38. The method of claim 30 , wherein the indication of ventricular proarrhythmia includes a time duration difference between a monitored Q–T interval and a selected duration range, a time duration difference between a Q–T interval monitored after initiating drug therapy delivery and a Q–T interval monitored prior to initiating drug therapy delivery, Q–T interval variability, and a frequency of ventricular ectopy.
39. The method of claim 30 , wherein the indication of ventricular proarrhythmia includes frequency of ventricular ectopy.
40. The method of claim 39 , further comprising internally terminating drug therapy delivery to the patient responsive to a frequency of ventricular ectopy exceeding a selected threshold frequency of ventricular ectopy after initiating drug therapy delivery.
41. The method of claim 39 , further comprising internally terminating drug therapy delivery to the patient responsive to a frequency of ventricular ectopy measured after initiating drug therapy delivery exceeds a frequency of ventricular ectopy measured prior to initiating drug therapy by at least 50%.Cited by (0)
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